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   nk细胞细胞毒 的翻译结果: 查询用时:0.46秒
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nk细胞细胞毒
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  “nk细胞细胞毒”译为未确定词的双语例句
     The refolded rhIL 18 enhanced the cytotoxicity of NK cells in the presence of IL 2(10 U/ml) in vitro.
     实验显示rhIL 18协同IL 2 (10U/ml)诱导NK细胞细胞毒活性。
短句来源
     Studying on the Construction of Eukaryotic Expression Vector of Human HLA-G Gene and the Suppression of Cytotoxic Action of NK Cell
     人HLA-G基因真核表达载体的构建及抑制NK细胞细胞毒作用的研究
短句来源
     Preparations of the rhIL 18 stimulates proliferation of T cells, induces secretion of IFNγ by the monocytes and lymphocytes in peripheral blood and enhances NK cytotoxicity of the PBMNCs.
     表达的rhIL 18蛋白具有促进T细胞增殖、增强NK细胞细胞毒作用及诱导外周血单核淋巴细胞合成IFN γ的能力 ,基本上具有天然IL 18相同的生物学活性。
短句来源
     Methods Porphyra polysaccharide in different dosages (0.025,0.050,0.150g·kg~(-1)) were injected intraperitoneally into the immunosuppressive mice induced by cyclophosphamide for 7d. On day 8,the cytotoxic activity of NK cells,the levels of interferon-γ(IFN-γ)and nitric oxide (NO)in the cultured supernatants of spleen cells were determided.
     方法小鼠腹腔注射不同剂量(0.025,0.050和0.150g.kg-1)的紫菜多糖,每日1次,连续7d,并在给予紫菜多糖的第1d,2d同时注射环磷酰胺造成免疫功能低下模型,第8d检测小鼠的NK细胞细胞毒活性,以及脾细胞分泌IFN-γ和NO的水平。
短句来源
     Results Preliminary studies showed that rhIL 18 GFP as well as rhIL 18 augmented T cell proliferation and IFN γ production by ConA stimulated human PBMCs, and enhanced NK cell cytotoxicity. In addition, rhIL 18,GFP has shown specific binding to P815 cells and the stained cells could be analyzed with flow cytometry.
     结果表达的rhIL-18及rhIL-18-GFP均具有促进T细胞增殖,增强NK细胞细胞毒作用及诱导外周血单核淋巴细胞合成IFN-γ的能力,rhIL-18-GFP还具有GFP的绿色荧光特性,可对P815细胞进行标记。
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  相似匹配句对
     Cytochalasin B
     细胞B
短句来源
     Cytotoxic T Cell
     细胞T细胞
短句来源
     2) the cytotoxic activity of NK cells in peripheral blood;
     2)外周血NK细胞活性;
短句来源
     blood NK cell's malicious activation of periphery;
     2)外周血NK细胞活性;
短句来源
     Preliminary Investigation of Murine NK Cytotoixc Kinetics
     小鼠NK细胞动力学的初步探讨
短句来源
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  natural killer cell cytotoxicity
Mean natural killer cell cytotoxicity mediated by enriched non-T cells from patients (37 ± 4.0%) was lower (p >amp;lt; 0.03) than in controls (56 ± 3.7%).
      
In in vitro experiments, the human natural killer cell cytotoxicity was investigated in the presence of pentoxifylline.
      
In the in vitro cytotoxicity reaction, pentoxifylline at a concentration of 100 μg/ml was found to suppress the natural killer cell cytotoxicity at any stage of the reaction.
      
Depression of murine natural killer cell cytotoxicity by isobutyl nitrite
      
The results showed that whilst natural killer cell cytotoxicity was only marginally depressed, mitogen responsiveness and lymphocyte participation in a mixed lymphocyte reaction were severely reduced 3-7 days post-cryosurgery.
      
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The affects of aclactnomycin B, adriamycin and berberine in vitro on cytotoxicity of human peripheral blood NK cells have been studied. The activity of NK cells was determined by detecting the changes of 51Cr release rate from 51Cr labelled K562 mye-ord leckamia cells after incubated with NK cells. After 1 hr exposure of NK cells to aclacmomycin B(0.5 and 1.0 μg/ml),adriamycin(0.5 and 1.0 μg/ml) and berberine(1.0 and 10μg/ml),no significant changes of 51Cr release rate were observed. It indicated that three...

The affects of aclactnomycin B, adriamycin and berberine in vitro on cytotoxicity of human peripheral blood NK cells have been studied. The activity of NK cells was determined by detecting the changes of 51Cr release rate from 51Cr labelled K562 mye-ord leckamia cells after incubated with NK cells. After 1 hr exposure of NK cells to aclacmomycin B(0.5 and 1.0 μg/ml),adriamycin(0.5 and 1.0 μg/ml) and berberine(1.0 and 10μg/ml),no significant changes of 51Cr release rate were observed. It indicated that three of drugs neither inhibited nor stimulated NK cell activity. Aclacinomycin B and berbenne seemed to have slight augmentation on the process of NK cell attacking target ceils at higher concentration, whereas adriamycin appeared a slightly inhibitory effects. Three drugs all anduced ancrease of spontaneous 51Cr release although at different level. So it was not easy to identify the anhibitory effect of adriamycin and enhancement of aclacinomycin B and berbenne. Their affects on NK cell activity have been discussed.

本文研究了阿克拉霉素B、阿霉素和小檗碱对人外周血NK细胞活性的影响.NK细胞活性由测定~(51)Cr从NK细胞作用的标记K562细胞的释放率来决定.阿克拉霉素B(0.5和1.Oμg/ml),阿霉素(0.5和1.0μg/ml)和小檗碱(1.0和10μg/ml)作用1小时后,未见对NK细胞活性有显著影响,提示三个药物可能即不明显抑制也不促进NK细胞的细胞毒作用.阿克拉霉素B和小檗碱在高浓度时表现轻微的促进作用,但阿霉素有轻微抑制作用.三个药物均有不同程度地增加靶细胞~(51)Cr的自然释放率,以阿霉素最强,提示有细胞膜毒性产生.因而尚难肯定阿克拉霉素B和小檗碱的NK细胞活性促进作用.

The purpose of this study is to observe how SPA (Staphylococcal protein A) and SAC (Staphylococcus aureus Cowan I) injected directly into tumorbearing mice in vivo have effects on morphological changes of their peritoneal macrophages, on cytotoxic activaties of theri splenic natural killer cells (NK cells), on macrophages against tumor cells and on direct cytotoxicity against tumor cells, through both release test of 125I—udR labeled tumor cell DNA and scanning electron microscopy. Our results demonstrated that...

The purpose of this study is to observe how SPA (Staphylococcal protein A) and SAC (Staphylococcus aureus Cowan I) injected directly into tumorbearing mice in vivo have effects on morphological changes of their peritoneal macrophages, on cytotoxic activaties of theri splenic natural killer cells (NK cells), on macrophages against tumor cells and on direct cytotoxicity against tumor cells, through both release test of 125I—udR labeled tumor cell DNA and scanning electron microscopy. Our results demonstrated that the macrophages were apparently activated after injecting SAC: they became 2—3 times in size as large as those of the control group; The surface folds and processes of these macrophages were remarkably enhanced. It seems to be that the cytotoxic activaties of the macrophages and NK cells augmented significantly by both SPA and SAC were consistent with the strength of their antitumor responses. these data sugest that the antitumor mechanisms of SPA injected directly in vivo may be related to the enhancement of macrophage and NK cell activaties, perhaps without the direct cytotoxicity of SPA against tumor cells.

本研究通过~(125)I-udR标记肿瘤细胞DNA释放试验和扫描电镜,观察了SPA和SAC直接体内注射对带瘤小鼠腹腔巨噬细胞细胞毒及其超微结构和脾脏NK细胞细胞毒的影响;SPA和SAC对瘤细胞的直接毒效应。结果表明,SAC治疗后巨噬细胞明显活化,其体积可达对照组的2—3倍,表面皱褶增多、增厚,有许多粗大的伪足;SPA和SAC均能使巨噬细胞、NK细胞、细胞毒活性显著增强,与抗肿瘤效应的强弱似呈一致关系;二者无直接瘤细胞毒效应。这些结果提示,葡萄球菌A蛋白体内注射的抗肿瘤机制与其增强巨噬细胞和NK细胞活性有关,而与直接瘤细胞毒作用无关。

The effects of the activition of SPA and SCA to peritoneal macrophages andsplenic NK cells were observed by DNA released assay of ~(125)I-udR labeled tumorcells. The result showed that SPA and SPC may enhanced the cytotoxic activities ofthe macrophages and NK cells odviously, but they hadn't direct cytotoxic effects.

本文通过~(125)Ⅰ-udR标记肿瘤细胞DNA释放试验观察了SPA和SAC直接体内注射对带瘤小鼠腹腔巨噬相胞细胞毒和脾脏NK细胞细胞毒的影响,SPA和SAC对瘤细胞的直接毒效应。结果表明,SPA和SAC均能使带瘤小鼠巨噬细胞、NK细胞细胞毒活性明显增强,二者无直接瘤细胞毒效应。这些提示葡萄球菌A蛋白体内注射的抗肿瘤机制与其增强巨噬细胞和NK细胞细胞毒活性有关,与直接瘤细胞毒作用无关。

 
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